Heart failure is one of the most widespread and devastating cardiac afflictions, currently affecting approximately 15 million people worldwide, including over 5 million in the United States. In the U.S., approximately 450,000 new patients are diagnosed with heart failure each year. One factor that contributes to heart failure is asynchronous activation of the ventricles such that the mechanical contraction is not coordinated effectively thus compromising cardiac function. As a result, the pumping ability of the heart is diminished and the patient experiences shortness of breath, fatigue, swelling, and other debilitating symptoms. The weakened heart is also susceptible to potentially lethal ventricular tachyarrhythmia. A decrease in cardiac function can result in a progression of heart failure. In many cases, pacing control parameters of the pacemaker or implantable cardioverter defibrillator (ICD) can be adjusted to help improve cardiac function and reduce the risk or degree of heart failure.
One particularly promising technique for reducing the risk of heart failure is cardiac resynchronization therapy (CRT). CRT seeks to normalize asynchronous cardiac electrical activation and the resultant asynchronous contractions by delivering synchronized pacing stimulus to both ventricles using pacemakers or implantable cardioverter defibrillators (ICDs) equipped with biventricular pacing capability. The stimulus is synchronized to help improve overall cardiac function. This may have the additional benefit of reducing the susceptibility to life-threatening tachyarrhythmias.
For example, within patients subject to left bundle branch block, pacing signals delivered to the left ventricle (LV) are timed relative to right ventricular pacing signals for the purpose of improving cardiac function. Briefly, within such patients, natural electrical signal nerve conduction pathways are damaged or blocked and so intrinsic pacing signals from the sinus node do not follow normal pathways through the left bundle branch and into the left ventricular myocardium to allow the LV to contract efficiently and uniformly. Instead, the electrical signals propagate through alternate pathways, particularly through the myocardium itself, resulting in different portions of the left ventricular myocardium contracting at different, less than appropriate or optimal times. Since the LV does not contract uniformly, its pumping efficacy is reduced and overall cardiac function is impaired.
With CRT, pacing pulses are delivered directly to the LV in an attempt to ensure that the left ventricular myocardium will contract more uniformly. A time delay relative to atrial pacing pulses and to right ventricular pacing pulses is set in an attempt to achieve optimal cardiac function. Typically, a right-ventricle left-ventricle (RV-LV) delay is initially set to zero while an atrioventricular (AV) delay (i.e. the pacing time delay between the atria and the ventricles) is adjusted to yield the best cardiac function. Then, the RV-LV delay is adjusted to achieve still further improvements in cardiac function. Within most patients, the RV-LV delay is set to a positive value, i.e. the LV is paced slightly before the right ventricle (RV). In other patients, the RV-LV delay is negative such that the RV is paced slightly before the LV. Similar techniques are also employed for patients whose nerve conduction pathways are corrupted due to right bundle branch block or due to other problems such as the development of scar tissue within the myocardium following a myocardial infarction.
With current state-of-the-art CRT techniques, the relative timing between left ventricular and right ventricular pacing pulses is adjusted in an attempt to improve cardiac function. Although such techniques are effective, it would be desirable to provide further improvements so as to achieve still greater benefits in cardiac function. In particular, whereas current CRT techniques are primarily directed to determining the optimal time delay between various pacing pulses, even greater potential improvement in overall cardiac function may be gained by also identifying the optimal pacing electrode locations for use in conjunction with CRT techniques.
Unfortunately, accurately determining that site can be a tedious and an often times lengthy effort with less than preferred results. Current approaches for trying to achieve optimized hemodynamics are quite varied and necessarily limited. Some physicians attempt to use electrocardiograms to identify an optimal site, by determining the LV site of the latest electrical delay. Some utilize arterial pressures to identify the best sites (which generally result in increased blood pressure). Others may use trans-esophageal echo (TEE) or tissue Doppler imaging (TDI) to try and find the site of last LV mechanical activation. More recently, some physicians are finding that a more precise method of finding the site of last LV mechanical activation may be to combine TDI and endocardial mapping technology. The last activated site within the LV is believed to be the optimal site for pacing because it corresponds to portions of the LV myocardium that would otherwise contract last in response to intrinsic pacing pulses and hence which most significantly contributes to uneven contraction of the chamber. By delivering pacing pulses directly at that location, adjacent portions of the myocardium can be caused to contract sooner, thus improving the uniformity of left ventricular contraction and thereby improving stroke volume from the LV and hence improving overall cardiac function.